The baroreflex regulates blood pressure through specialized nerve cells called baroreceptors that sense increases or decreases in blood pressure. Baroreceptors send signals to the brain that indicate whether heart rate and vascular tone (i.e., constriction of arterioles and veins in the peripheral vascular system) should be increased, decreased or kept constant in response to changes in blood pressure. For example, when a person stands from a seated or supine position, gravity forces blood to pool in the lower extremities. Blood pressure drops momentarily while signals from baroreceptors are received and processed by the brainstem, which increases heart rate and vascular tone to reestablish a nominal blood pressure. If the body does not properly compensate for the shift in blood volume, known as orthostatic hypotension, a person may experience syncope (i.e., fainting, passing out).
It is important for a medical practitioner evaluating a patient who has suffered a syncopal episode to determine the cause of the episode, so that the patient may be properly treated. For example, syncope may be caused by an inadequate baroreflex due to emotional stress, pain, shock, orthostatic stress, overheating, dehydration, exhaustion, violent coughing spells, medications and other drugs (e.g., beta-blockers, alcohol), and adrenal insufficiency, as well as a wide variety of cardiac, neurologic, psychiatric, metabolic and lung disorders. Initial treatment for an inadequate baroreflex is administration of intravenous fluids to increase blood volume. However, administration of fluids may be improper when syncope is caused by a non-baroreflex related event, such as edema or congestive heart failure.
To distinguish between baroreflex and non-baroreflex related events, a patient's “orthostatics” are measured. In a typical measurement, a patient lies flat for approximately five minutes. Basal blood pressure and pulse are obtained in this supine position. The patient is then asked to sit with feet dangling or to stand, and their blood pressure and pulse are taken a second time. The patient may remain sitting or standing for a minute or two and blood pressure and pulse may be taken a third time. When a patient is incoherent or unable to sit or stand unaided, the patient may be secured to a tilt-table for the purpose of performing the orthostatic stress test. A sustained increase in pulse of twenty beats per minute or a decreased systolic pressure of more than 20 mmHg is considered a positive indication of an inadequate baroreflex.
Orthostatic measurements are designed to detect the absence of a sufficient baroreflex (i.e., to test a null hypothesis), and they may be inaccurate if blood pressure and pulse measurements are taken too slowly. The measurements are thus subject to human error and variation among practitioners. In the absence of objective and affirmative data showing the presence of a physiological response, practitioners frequently request additional and often expensive tests, such as electroencephalography (EEG), magnetic resonance (MR) or computed tomography (CAT) brain scans, and electrocardiography (EKG) during workup of syncopal episodes.
In the above mentioned orthostatic test, the patient's pulse may be monitored using a pulse oximeter, which is an optical device that attaches to a patient's finger, ear or other thinly skinned body part, to measure blood oxygen saturation and pulsatile flow (i.e., heart rate). The pulse oximeter shines two colors of light onto the skin that are absorbed differently by hemoglobin in the blood depending on whether the hemoglobin is oxygenated or deoxygenated. The amount of light absorption is used to calculate the percentage of oxygenated hemoglobin in the blood (i.e., blood oxygen saturation). A photoplethysmogram (PPG) can be generated by measuring the change in light absorption caused by volumetric changes within the perfused skin.
Volumetric changes in skin perfusion result from a combination of cardiac and respiratory pressure effects, as well as vascular resistance of the skin. Cardiac pressure, which varies as the heart contracts and expands with each heartbeat, is attenuated by respiration which varies intrapleural pressure, i.e., the pressure between the thoracic wall and the lungs. This respiratory effect is often referred to as Respiratory Induced Variation (RIV). During inspiration, intrapleural pressure decreases by up to 4 mmHg, which distends the right atrium, allowing for faster filling and increased stroke volume. This increased stroke volume means that more blood leaves the venous pool and is accommodated in the central pool. Conversely, during exhalation, the heart is compressed, decreasing cardiac efficiency and reducing stroke volume. Blood from the central pool is forced into the venous plexus. RIVs vary between individuals and each individual's RIV varies with the tidal volume of each respiration.
Analysis of PPG data for the types of features discussed above has historically been performed using frequency-domain or time-domain signal processing techniques. Frequency-domain techniques provide average values of features, such as average heart rate, while time-domain techniques allow for the extraction of features such as pulse height and instantaneous heart rate. Additionally, an RIV may be plotted by connecting one point (e.g., the peak or valley) from each of a series of cardiac pulses to create an envelope, i.e., a curve tangent to each of a family of curves or lines. The observed RIV envelope rises and falls with a frequency corresponding to respiratory rate rather than heart rate.